hiv - everything you need to know 3
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8/14/2019 HIV - Everything You Need to Know 3
1/1
11/15/13 HIV - Wikipedia, the free encyclopedia
en.wikipedia.org/wiki/Human_immunodeficiency_virus 3/19
Diagram of the immature and mature
forms of HIV
is broken down by a cellular protease to form gp120 and gp41. The six remaining genes, tat, rev, nef, vif, vpr,
and vpu(or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect
cells, produce new copies of virus (replicate), or cause disease.[14]
The two Tat proteins (p16 and p14) are transcriptional transactivators for the LTR promoter acting by binding
the TAR RNA element. The TAR may also be processed into microRNAs that regulate the apoptosis genes
ERCC1 and IER3.[17][18]The Rev protein (p19) is involved in shuttling RNAs from the nucleus and the
cytoplasm by binding to the RRE RNA element. The Vif protein (p23) prevents the action of APOBEC3G (acell protein that deaminates DNA:RNA hybrids and/or interferes with the Pol protein). The Vpr protein (p14)
arrests cell division at G2/M. The Nef protein (p27) down-regulates CD4 (the major viral receptor), as well as
the MHC class I and class II molecules.[19][20][21]
Nef also interacts with SH3 domains. The Vpu protein (p16) influences the release of new virus particles from
infected cells.[14]The ends of each strand of HIV RNA contain an RNA sequence called the long terminal
repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by
proteins from either HIV or the host cell. The Psi element is involved in viral genome packaging and recognized
by Gag and Rev proteins. The SLIP element (TTTTTT) is involved in the frameshift in the Gag-Pol reading
frame required to make functional Pol.[14]
Tropism
Main article: HIV tropism
The term viral tropism refers to the cell types a virus infects. HIV can
infect a variety of immune cells such as CD4+T cells, macrophages,
and microglial cells. HIV-1 entry to macrophages and CD4+T cells is
mediated through interaction of the virion envelope glycoproteins(gp120) with the CD4 molecule on the target cells and also with
chemokine coreceptors.[15]
Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing
strains (NSI) use the-chemokine receptor CCR5 for entry and are,
thus, able to replicate in macrophages and CD4+T cells.[22]This
CCR5 coreceptor is used by almost all primary HIV-1 isolates
regardless of viral genetic subtype. Indeed, macrophages play a key
role in several critical aspects of HIV infection. They appear to be the
first cells infected by HIV and perhaps the source of HIV productionwhen CD4+cells become depleted in the patient. Macrophages and
microglial cells are the cells infected by HIV in the central nervous
system. In tonsils and adenoids of HIV-infected patients,
macrophages fuse into multinucleated giant cells that produce huge
amounts of virus.
T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+T cells as well as in macrophages
and use the -chemokine receptor, CXCR4, for entry.[22][23][24]Dual-tropic HIV-1 strains are thought to be
transitional strains of HIV-1 and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.
The -chemokine SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this
by down-regulating the expression of CXCR4 on the surface of these cells. HIV that use only the CCR5
receptor are termed R5; those that use only CXCR4 are termed X4, and those that use both, X4R5. However,
the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on
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